2024 Asia Conference on Lung Cancer (ACLC) - Poster & ePosters-PP01.22

PP01.22 - Zuoqing Song

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This study investigates the role of resveratrol in mitigating platelet activation induced by non-small cell lung cancer (NSCLC) and its potential as a treatment strategy to combat cancer-associated venous thromboembolism (CAT). The research analyzed clinical data and employed A549 human lung cancer cells and Lewis mouse lung cancer cells to study tumor-induced platelet activation and the effects of resveratrol. Various methods, such as Western blotting, electron microscopy, flow cytometry, and ELISA, were used to assess the protein expression, morphology of extracellular vesicles (EVs), platelet activation, reactive oxygen species (ROS), and secretory protein quantification.<br /><br />Key findings indicate that resveratrol can alleviate lung cancer-induced ferroptosis, associated with platelet activation. The study highlights that NSCLC patients commonly exhibit a hypercoagulable state, and lung cancer cells can trigger platelet activation. However, resveratrol exerts an attenuation effect on this platelet activation. It was discovered that resveratrol prompts lung cancer cells to secrete HMGB1-enriched EVs, which facilitate platelet ferroptosis and limit platelet activation by escalating ROS levels, lipid peroxidation, and disrupting cystine transporters.<br /><br />In vivo experiments reinforced these findings, showing that resveratrol suppresses lung cancer cell proliferation and inhibits platelet activation induced by tumors in mice. This research suggests that resveratrol, a natural compound with previously reported anti-tumor effects, could offer a novel pharmacological approach for preventing and treating lung cancer and associated thromboembolic complications. Overall, the study sheds light on resveratrol’s potential mechanism of action in promoting ferroptosis-mediated platelet inactivation, thereby presenting an innovative path for further exploration in cancer therapies.

Keywords

resveratrol

platelet activation

non-small cell lung cancer

venous thromboembolism

A549 cells

Lewis mouse cells

extracellular vesicles

reactive oxygen species

ferroptosis

HMGB1